Nutritional Attributes of Cereal Grains And Legumes as Functional Food: A Review
Megh R. Goyal, Durgesh Nandini Chauhan in Plant- and Marine-Based Phytochemicals for Human Health, 2018
The unsaturated fats such as linoleic and oleic acid in oats are reported to be higher as compared to other cereal grains.55, 119 It is enriched with various phenolic compounds such as vanillic, p-coumaric, caffeic, hydroxybenzoic acid, and their derivatives.31 Different oat-specific derivatives of hydroxycinnamic acid such as avenanthramides and avenalumic acids have been found specifically in oats as compared to other cereals.95, 152 Three different avenanthramides mostly found in oats are: 2c, 2p, and 2f where 2 represents 5-hydroxyanthranilic acid and c, p, and f represent caffeic, p-coumaric, and ferulic acid, respectively.152 β-D-glucan also known as β-glucan is composed of β-(1–4)-linked glucose units, separated by β-(1–3)-linked glucose units. As a dietary fiber, it also has antioxidant properties.23 It has also been reported for lowering cholesterol,113 insulin, and glucose as well as further reduction in growth of heart disease and type II diabetes.113 This cholesterol-lowering effect is due to increased viscosity of intestinal contents.7
Pathophysiology of Diabetes
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
Glucose is a molecule made up of six carbons. It is a very efficient form of fuel for the body. When metabolized in the presence of oxygen, it is broken down to form carbon dioxide and water. The brain and nervous tissues use glucose as the source of most of their required energy. Other tissues and organ systems use fatty acids and ketones as fuel. The brain is unable to synthesize or store sufficient glucose to last for more than several minutes. A continual glucose supply from the systemic circulation is required for the cerebrum to function normally. Brain death can be due to severe and prolonged hypoglycemia. Significant brain dysfunction occurs because of only moderate hypoglycemia. Glucose is obtained from the circulation by tissues. Hypoglycemia is extremely dangerous in comparison to hyperglycemia. There is rigid control of blood glucose levels while fasting, and they remain between 70 and 99 mg/dL, which is equivalent to between 4.0 and 5.5 mmol/L. After eating, blood glucose levels rise. Insulin is released from the beta cells of the pancreas, allowing glucose to be transported into the body cells. Approximately 66% of the glucose contained in each meal is removed from the blood, and stored in the liver or skeletal muscles as glycogen. When the liver and skeletal muscles become saturated with glycogen, remaining glucose is converted into fatty acids by the liver. These are stored as triglycerides in the adipose tissue’s fat cells.
Clinical Problems Associated with Diabetes Mellitus
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla in Heart Dysfunction in Diabetes, 2019
Glucose is needed by the cell for energetic and biosynthetic reasons. The extracellular concentration of glucose is higher than the intracellular levels. Glucose can enter the cell without the need for insulin; however, insulin greatly facilitates this entry process. Insulin does this by increasing the Vmax for glucose transport without altering the affinity of the transporter.53 This increase in the maximum velocity of glucose transport by insulin may not be due to a change in mobility of a fixed number of transport systems but instead may reflect an increase in the number of the glucose transport systems.54 Earlier work has suggested that insulin or some fragment of it may be internalized and exert some intracellular action which would stimulate glucose entry. This is probably inaccurate and it is more likely that the binding of insulin to the receptor results in a more active complex.55 This is reinforced by data which show that vanadate may stimulate glucose transport in an insulin-dependent manner.56
Impact of biotin supplemented diet on mouse pancreatic islet β-cell mass expansion and glucose induced electrical activity
Published in Islets, 2022
Israel Morales-Reyes, Illani Atwater, Marcelino Esparza-Aguilar, E. Martha Pérez-Armendariz
Diabetes includes various pathologies that have as a common sign hyperglycemia. Diabetes type 2 (DT2) represents 90% of the diabetes cases and constitutes a pandemic with an increasing global prevalence.1 Insulin is the only hormone capable of reducing serum glucose levels. This hormone is exclusively produced by β-cells, which constitute the main central mass in a pancreatic islet (~80% in the mouse). Glucose is a key physiological stimulus for β-cell electrical activity, which is critical for adequate insulin secretion. In mouse islet β-cells, glucose between 0 and 7.5 mM depolarizes the membrane by inhibition of KATP ionic channels. Between 7.5 and 16.0 mM, glucose induces slow membrane potential (Vm) oscillations. Vm rhythmically alternates between a silent phase (Sph) (~ −55 mV) and a more depolarized or active phase (Aph) (~ −45 mV), where action potentials (APs) are generated. The APs result from the activation of voltage dependent Ca2+ and K+ channels. The duration of the Aph and, the frequency of the APs, increases in a glucose concentration-dependent manner from 7.0 to 22.0 mM.2–4 Due to the high incidence of electrical coupling, as demonstrated in freshly isolated pairs of double voltage clamped β-cells5,6, as well as in perfused islets,7,8 the slow Vm oscillations occur in synchrony and in phase in most islet β-cells.9 The synchrony and phase in the electrical activity determines that the islet secretes insulin in a pulsatile manner at the same frequency.10
Melatonin promotes self-renewal of nestin-positive pancreatic stem cells through activation of the MT2/ERK/SMAD/nestin axis
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Chunyu Bai, Yuhua Gao, Xiangyang Zhang, Wancai Yang, Weijun Guan
A key functional feature of beta cells is its ability to repeatedly perform glucose-stimulated insulin secretion. Beta cells challenged sequentially with 5.5, 20.5, 5.5, 20.5, 5.5 and 20.5 mM glucose, with a 30 min incubation for each concentration. After sequential low/high-glucose challenges, insulin concentration were analyzed in supernatant using ELISA. And glucose-induced insulin secretion demonstrated that PSCs derived from beta cells could release insulin at glucose concentrations of 5.5 mM and 20.5 mM. Analysis of glucose-induced insulin secretion demonstrated that beta cells derived with different combinations of inducers could release insulin, while undifferentiated progenitor cells (G1) did not release insulin. The box plots show that insulin secretion increased when the glucose concentration increased in G2–G7, when the secreted insulin amounts of IPCs differentiation from PSCs was assessed, the combination of nicotinamide, HGF, and active-A-induced IPCs secretion at a higher efficiency compared with combinations of melatonin (Figure 10). These validation results were largely in agreement with the data of IPCs differentiation.
Evidence for the existence and potential roles of intra-islet glucagon-like peptide-1
Published in Islets, 2021
Scott A. Campbell, Janyne Johnson, Peter E. Light
Glucose is an essential regulator of islet hormone secretion. Both beta and delta cells rely on glucose-stimulated secretion pathways, where hyperglycemia favors the release of insulin and somatostatin from the islet. In beta and delta cells, glucose entry and metabolism results in the closure of KATP channels, membrane depolarization, elevated intracellular calcium, and hormone secretion. This pathway in delta cells is more dependent on calcium-induced Ca2+ release, whereas beta cells depend on the activation of voltage-gated Ca2+ channels.60 The sodium-glucose transporter SGLT2 is expressed in 33–58% of human delta cells, and its current contributes to insulin-induced somatostatin secretion.108 In the presence of SGLT2 inhibitors like dapagliflozin, insulin-stimulated somatostatin secretion is modestly suppressed.108,109 As previously stated, the actions of GLP-1 in alpha cells are also glucose-dependent. In hyperglycemia, GLP-1R activation inhibits alpha cell hormone release, while receptor activation in hypoglycemia potentiates hormone secretion.100